Researchers at The Jackson Laboratory, Broad Institute, and Yale executed a massively parallel reporter assay testing over 220,000 single‑nucleotide variants across five human cell types, resolving functional effects for roughly 20% of previously implicated genomic regions. The work, published in Nature, links specific noncoding changes to regulatory activity tied to blood pressure, cholesterol, glucose and other traits. The team used high‑throughput reporter constructs to score variant regulatory potential at scale and validated dozens of causal alleles, providing higher‑resolution targets for downstream mechanistic studies and therapeutic hypothesis generation. Authors framed the dataset as a bridge from genome‑wide association signals to actionable biology. For geneticists and drug developers, these maps narrow candidate causal variants and can de‑risk target selection by indicating which alleles alter gene regulation in disease‑relevant cell contexts. The approach also highlights how multiplexed functional screens accelerate the path from association to biology.